Objectives Antibody response to the first dose of BNT162b2 SARS‐CoV‐2 is greater in COVID‐19‐convalescent than in infection‐naïve individuals. However, there are no data about T‐cell response in individuals with pre‐existing cellular immunity. Methods We evaluated T‐cell responses in parallel with SARS‐CoV‐2 antibody level after first dose of BNT162b2 vaccine in 23 infection‐naïve and 27 convalescent healthcare workers (HCWs) previously included in a study about humoral and T‐cell immunity. Results Overall, the antibody response was lower in the infection‐naïve group than in convalescent individuals (18 895 vs 662.7 AU mL −1 , P < 0.001), and intermediate but significantly lower in convalescent HCWs with previous negative serology (25 174 vs 1793 AU mL −1 ; P = 0.015). Indeed, anti‐spike IgG titres after the first dose correlated with baseline anti‐nucleocapsid IgG titres (rho = 0.689; P < 0.001). Pre‐existing T‐cell immunity was observed in 78% of convalescent and 65% of the infection‐naïve HCWs. T‐cell response after the first dose of the vaccine was observed in nearly all the cases with pre‐existing T‐cell immunity, reaching 94% in convalescent HCWs and 93% in those with cross‐reactive T cells. It was lower in the infection‐naïve group (50%; P = 0.087) and in convalescent HCWs with negative serology (56%; P = 0.085). Notably, systemic reactogenicity after vaccination was mainly observed in those with pre‐existing T‐cell immunity ( P = 0.051). Conclusion Here, we report that the first dose of BTN162b2 elicits a similar S‐specific T‐cell response in cases of either past infection or cross‐reactive T cells, but lower in the rest of infection‐naïve individuals and in convalescent HCWs who have lost detectable specific antibodies during follow‐up.

Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2) infection induces elevated levels of inflammatory cytokines, which are mainly produced by the innate response to the virus. The role of NK cells, which are potent producers of IFN-γ and cytotoxicity, has not been sufficiently studied in the setting of SARS-CoV-2 infection. We confirmed a different distribution of NK cell subsets in hospitalized COVID-19 patients despite their NK cell deficiency. The impairment of this innate defense is mainly focused on the cytotoxic capacity of the CD56dim NK cells. On the one hand, we found an expansion of the CD56dimCD16neg NK subset, lower cytotoxic capacities, and high frequencies of inhibitory 2DL1 and 2DL1/S1 KIR receptors in COVID-19 patients. On the other hand, the depletion of CD56dimCD16dim/bright NK cell subsets, high cytotoxic capacities, and high frequencies of inhibitory 2DL1 KIR receptors were found in COVID-19 patients. In contrast, no differences in the distribution of CD56bright NK cell subsets were found in this study. These alterations in the distribution and phenotype of NK cells might enhance the impairment of this crucial innate line of defense during COVID-19 infection.

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Objective T-cell responses against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are observed in unexposed individuals. We evaluated the impact of this pre-existing cellular response on incident SARS CoV-2 infections. Methods Follow up study of 38 seronegative health care workers (HCWs) with previous evaluation of CD8+ and CD4+ T-cell response after stimulation with SARS-CoV-2 structural proteins. Infection was considered in presence of a positive reverse transcription (RT)-PCR test and/or confirmed seroconversion. Results Twenty of the 38 HCWs included (53%) had a previous specific CD8+ T cell response to peptides encompassing the spike (S) protein in 13 (34%), the membrane (M, 17, 45%), or/and the nucleocapsid (N, 3, 8%). During a follow up of 189 days (interquartile range, IQR, 172 to 195), 11 (29%) HCWs had a RT-PCR positive test (n=9) or seroconverted (n=2). Median duration of symptoms was 2 days (IQR, 0-7), and time to negative RT-PCR was 9 days (IQR, 4-10). Notably, six incident infections (55%) occurred in HCWs with pre-existing T-cell response (30% of those with cellular response), who showed a significant lower duration of symptoms (three were asymptomatic). Three of the six HCWs having previous T-cell response continued testing seronegative. All the infected patient developed a robust T-cell response to different structural SARS-CoV-2 proteins, especially to protein S (91%). Conclusion Pre-existing T-cell response does not seems to reduce incident SARS-CoV-2 infections, but it may contribute to asymptomatic or mild disease, rapid viral clearance and differences in seroconversion.

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